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The epigenetics life history and metabolic diseases

Changes in the interaction between the promoter and enhancer supports the epigenetic regulation of Ctsc maternal malnutrition, diet-induced rat pancreatic islet transcription factors.Impaired growth in neonatal rats by pancreatic islet beta-cell dysfunction related to epigenetic modification of the normalization of the incretin insulin analogues can reverse the incidence of type 2 diabetes (T2DM) locus.Apparent there is a strong correlation between genetic type and later obesity, genetic type of Ctsd maternal nutrition and on behalf of concept in human birth.Type 2 diabetes and obesity Epigenetics of the lifetime risk of type 2 diabetes in a human presymptomatic indicators.Phenotypic effect of the early life of excess nutrients, the mice through the paternal intergenerational transmission.Clinical and experimental studies have shown that Ctse early life experiences can be the lifetime risk of suffering from metabolic dysfunction, perhaps through epigenetic mechanisms may span multiple generations. The data released in 2011 showed that the epigenetic analysis may serve as early markers of metabolic disease, and early in life prevention become possible.

Population and individual differences can lead to different susceptibility to environmentally induced fat. Genome-wide association studies to explain this difference has been disappointing, and we are now increasingly focused on the possible epigenetic interpretation. Epigenetic changes may be early in CTSF life began. A wide range of human experimentation, clinical and epidemiological evidence shows that the development of early life factors (including maternal diet, and then exposed in the development of the specification range) impact the incidence of metabolic diseases later in life risk. This phenomenon is sometimes called developmental programming.Because of the lack of a reasonable biological mechanism, the early discovery has largely been ignored, but the interpretation developed in the past decade has been framed in the development of plasticity - adaptive process allows organisms are able to CTSH life respond to early environmental cues and adjust their developmental trajectories.Developmental plasticity at least by epigenetic mechanisms (including DNA methylation and histone modifications) section be supported. A large number of papers published in 2011, strengthening the reliability of these conclusions.Previous comprehensive studies show that malnourished rats by their mothers during pregnancy and lactation may develop in adulthood as insulin resistance and obesity phenotype. Furthermore, the lack of transcription factor hepatocyte nuclear factor 4α (HNF-4α, the key regulator of pancreatic islet β-cell gene expression) in mice existence of impaired glucose tolerance. How 2011, Sandovici et al reported in rat maternal diet affect future generations of epigenetic regulation of pancreatic β cells of HNF-4α gene locus. The researchers found that rat maternal low-protein diet led to low offspring islet Hnf4a gene expression. The level of the molecular mechanism of this low expression attributed in part to Hnf4a gene enhanced the promoter region of histone modifications, the resulting ring of chromatin changes, and ultimately enhance the interaction between the sub-region and the specific promoter region was weakened. Body of the normal age-dependent Hnf4a point epigenetic silencing in utero exposure to low-protein diet in rats is more serious. These data contribute to the growing number of experiments on the the epigenetics results from the relevant organizations of the metabolism in early life malnutrition literature.